Inflammation contributes importantly to atherosclerosis, but detection in humans is limited to surrogate inflammatory markers in blood. We hypothesized that arterial inflammation would increase MRI-determined wall thickness, T2-weighted signal intensity, and gadolinium contrast enhancement due to increased tissue water, cellular infiltration, and vasovasorum dilation or neovascularization, and that those MRI features would be reflected in elevated serum markers of inflammation. To this end, 68 subjects were studied: 17 healthy subjects 18-30 years of age. All other subjects were 40 years or older, including 17 with coronary artery disease, 17 healthy subjects with LDL cholesterol greater than 160 mg/dl, and 17 healthy subjects with normal lipid levels. Double inversion recovery fast spin echo sequence images of the common carotid arteries and infrarenal aorta were obtained at 1.5T before and after gadolinium-DTPA (0.1 mmol/kg) contrast to quantitatively assess the arterial walls for evidence of inflammation. An MRI scan was determined as abnormal if wall thickness, T2-weighted signal intensity, and/or contrast enhancement values were greater than 2 SD from normal values. In the 51 subjects 40 years of age or older, 22 had abnormal scans, including including increases in wall thickness (14), T2-weighted signal intensity (11) and/or gadolinium contrast enhancement (7). Ten subjects in this group had focal plaques in the carotid arteries (5) and/or aorta (6).Compared with the remaining subjects (none of whom had focal plaques), these 22 had significantly higher levels (mean +/- SEM)of vascular cell adhesion molecule (572+/-32 vs. 471+/-25 ng/mL, p=0.01), intercellular adhesion molecule (244+/-18 vs. 202+/-24 ng/mL, p=0.01),interleukin-6 (3.5+/-0.5 vs. 2.0+/-0.6 pg/mL, p<0.01)and C-reactive protein (0.56+/-0.23 vs. 0.30+/-0.11 mg/dL, p=0.02. Nine of 22 subjects were detected based on T2 or contrast enhancement abnormalities of the arterial wall in the absence of wall thickness abnormalities. Almost all MRI parameters were significantly different between the younger normals and older healthy subjects, indicating the need for age-matched controls as in this study.We conclude that MRI characteristics of large arteries may permit in vivo noninvasive detection of vascular inflammation, even in apparently healthy middle-aged and older subjects. Thus, MRI of arteries may provide a new approach to regionally investigate the contribution of inflammation to atherogenesis.